1. Field of Inventions
The present inventions relate generally to structures for positioning diagnostic and therapeutic elements within the body and, more particularly, to devices which are particularly well suited for the treatment of cardiac conditions.
2. Description of the Related Art
There are many instances where diagnostic and therapeutic elements must be inserted into the body. One instance involves the treatment of cardiac conditions such as atrial fibrillation and atrial flutter which lead to an unpleasant, irregular heart beat, called arrhythmia.
Normal sinus rhythm of the heart begins with the sinoatrial node (or “SA node”) generating an electrical impulse. The impulse usually propagates uniformly across the right and left atria and the atrial septum to the atrioventricular node (or “AV node”). This propagation causes the atria to contract in an organized way to transport blood from the atria to the ventricles, and to provide timed stimulation of the ventricles. The AV node regulates the propagation delay to the atrioventricular bundle (or “HIS” bundle). This coordination of the electrical activity of the heart causes atrial systole during ventricular diastole. This, in turn, improves the mechanical function of the heart. Atrial fibrillation occurs when anatomical obstacles in the heart disrupt the normally uniform propagation of electrical impulses in the atria. These anatomical obstacles (called “conduction blocks”) can cause the electrical impulse to degenerate into several circular wavelets that circulate about the obstacles. These wavelets, called “reentry circuits,” disrupt the normally uniform activation of the left and right atria.
Because of a loss of atrioventricular synchrony, the people who suffer from atrial fibrillation and flutter also suffer the consequences of impaired hemodynamics and loss of cardiac efficiency. They are also at greater risk of stroke and other thromboembolic complications because of loss of effective contraction and atrial stasis.
Although pharmacological treatment is available for atrial fibrillation and flutter, the treatment is far from perfect. For example, certain antiarrhythmic drugs, like quinidine and procainamide, can reduce both the incidence and the duration of atrial fibrillation episodes. Yet, these drugs often fail to maintain sinus rhythm in the patient. Cardioactive drugs, like digitalis, Beta blockers, and calcium channel blockers, can also be given to control the ventricular response. However, many people are intolerant to such drugs. Anticoagulant therapy also combats thromboembolic complications, but does not eliminate them. Unfortunately, pharmacological remedies often do not remedy the subjective symptoms associated with an irregular heartbeat. They also do not restore cardiac hemodynamics to normal and remove the risk of thromboembolism.
Many believe that the only way to really treat all three detrimental results of atrial fibrillation and flutter is to actively interrupt all of the potential pathways for atrial reentry circuits.
One surgical method of treating atrial fibrillation by interrupting pathways for reentry circuits is the so-called “maze procedure” which relies on a prescribed pattern of incisions to anatomically create a convoluted path, or maze, for electrical propagation within the left and right atria. The incisions direct the electrical impulse from the SA node along a specified route through all regions of both atria, causing uniform contraction required for normal atrial transport function. The incisions finally direct the impulse to the AV node to activate the ventricles, restoring normal atrioventricular synchrony. The incisions are also carefully placed to interrupt the conduction routes of the most common reentry circuits. The maze procedure has been found very effective in curing atrial fibrillation. However, the maze procedure is technically difficult to do. It also requires open heart surgery and is very expensive. Thus, despite its considerable clinical success, only a few maze procedures are done each year.
Maze-like procedures have also been developed utilizing catheters which can form lesions on the endocardium to effectively create a maze for electrical conduction in a predetermined path. Exemplary catheters are disclosed in U.S. Pat. Nos. 6,013,052, 6,203,525, 6,214,002 and 6,241,754. Typically, the lesions are formed by ablating tissue with an electrode carried by the catheter. Electromagnetic radio frequency (“RF”) energy applied by the electrode heats, and eventually kills (i.e. “ablates”), the tissue to form a lesion. During the ablation of soft tissue (i.e. tissue other than blood, bone and connective tissue), tissue coagulation occurs and it is the coagulation that kills the tissue. Thus, references to the ablation of soft tissue are necessarily references to soft tissue coagulation. “Tissue coagulation” is the process of cross-linking proteins in tissue to cause the tissue to jell. In soft tissue, it is the fluid within the tissue cell membranes that jells to kill the cells, thereby killing the tissue.
Catheters used to create lesions (the lesions being 3 to 15 cm in length) typically include a relatively long and relatively flexible body portion that has one or more electrodes at or near its distal end. The portion of the catheter body portion that is inserted into the patient is typically from 23 to 55 inches in length and there may be another 8 to 15 inches, including a handle, outside the patient. The proximal end of the catheter body is connected to the handle which includes steering controls. The length and flexibility of the catheter body allow the catheter to be inserted into a main vein or artery (typically the femoral artery), directed into the interior of the heart, and then manipulated such that the electrode contacts the tissue that is to be ablated. Fluoroscopic imaging is used to provide the physician with a visual indication of the location of the catheter.
More recently, surgical soft tissue coagulation probes that carry one or more electrodes on relatively short, stiff shafts have been developed. Exemplary surgical probes are disclosed in U.S. Pat. No. 6,142,994. These probes may be used in endocardial and epicardial procedures where access to the heart is obtained by way of a thoracostomy, thoracotomy or median stemotomy. Such probes also allow endocardial lesions to be formed as a secondary procedure during a primary open heart surgical procedure such as mitral valve replacement, aortic valve replacement, and coronary artery bypass grafting.
Tissue temperature can be an issue in any lesion creation procedure. For example, a relatively wide deep lesion may be created by reducing the temperature of the tissue closest to the electrode. This shifts the hottest iso-thermal region deeper into the tissue, thereby enabling higher power to be delivered without causing char or excessive surface desiccation to occur. Higher power, in turn, results in a larger volume of tissue being heated to a temperature sufficient to coagulate tissue (above 50° C.) and, therefore, a wider and deeper lesion.
One method of reducing tissue temperature is to apply an electrically conductive cooling fluid to the tissue during a lesion formation procedure. The application of cooling fluid directly to tissue can, however, be problematic. It is very difficult to control the location of the cooling fluid on a beating heart because of the movement associated with beating and the curvature of the surface of the heart. It is also difficult to control the rate at which the fluid is delivered to the heart surface. The electrically conductive cooling fluid can, therefore, move to unintended areas. This makes it difficult to form the relatively narrow lesions that are preferred in epicardial and endocardial applications and leads to the coagulation of tissue other than the targeted tissue. The coagulation of non-targeted tissue is particularly problematic when lesions are being formed near nervous tissue such as the phrenic nerve.
Another method of reducing tissue temperature, which has been introduced in the catheter context, is the so-called “cooled tip” method. Here, a cooling medium is applied to the inner surface of a metallic tip electrode during a lesion formation procedure. Although the cooled tip method has proven to be an advance in the art, the use of tip electrodes is not always desirable. For example, elongate lesions must be formed by dragging a tip electrode along the tissue surface, which is slow and can result in gaps of conductive tissue that remain after the procedure is completed.
Accordingly, the inventor herein has determined that conventional methods of reducing tissue temperature are susceptible to improvement and, in particular, that a need exists for an apparatus including a cooled energy transmission device which is capable of forming an elongate lesion without being dragged or otherwise moved along the tissue surface.